实用药物与临床
實用藥物與臨床
실용약물여림상
PRACTICAL PHARMACY AND CLINICAL REMEDIES
2014年
10期
1236-1239
,共4页
于冬梅%张倩%周锦%曹惠鹃%张铁铮
于鼕梅%張倩%週錦%曹惠鵑%張鐵錚
우동매%장천%주금%조혜견%장철쟁
羟丁酸钠%8-异前列腺素%脂质过氧化作用%心肌缺血再灌注损伤
羥丁痠鈉%8-異前列腺素%脂質過氧化作用%心肌缺血再灌註損傷
간정산납%8-이전렬선소%지질과양화작용%심기결혈재관주손상
Gamma-hydroxybutyrate%8-isoprostane%Lipid peroxidation%Myocardial ischemia reperfusion injury
目的:比较不同剂量羟丁酸钠对离体大鼠缺血再灌注损伤心肌脂质过氧化作用的影响。方法将24只成年Wistar大鼠随机分为4组(n=6):心肌缺血再灌注组(I/R组),1 mmol/L羟丁酸钠组(RL组),2.5 mmol/L羟丁酸钠组( RM组),10 mmol/L羟丁酸钠组( RH组)。采用 Langendorff离体心脏缺血再灌注模型,四组均以K-H液平衡灌注10 min,再以K-H液及1、2.5、10 mmol/L羟丁酸钠的K-H液分别灌注10 min,然后全心停止灌注25 min,再分别继续灌注30 min。测定冠脉流出液总乳酸脱氢酶( LDH)活性;灌注末,用2.5%戊二醛固定左室心肌组织,观察心肌超微结构;留取心尖部心肌组织以检测8-异前列腺素、超氧化物歧化酶(SOD)活性。结果与IR组比较,RL组8-异前列腺素含量、SOD及LDH活性差异均无统计学意义(P>0.05),超微结构也未见损伤减轻;RM组8-异前列腺素含量、SOD活性差异均无统计学意义(P>0.05),LDH活性差异有统计学意义(P<0.05),超微结构可见损伤减轻;RH组8-异前列腺素含量、LDH活性升高(P<0.05),SOD活性差异均无统计学意义(P>0.05),超微结构可见损伤加重。结论羟丁酸钠(1、2.5 mmol/L)不能降低心肌缺血再灌注损伤大鼠的8-异前列腺素含量,抑制脂质过氧化反应;但是2.5 mmol/L羟丁酸钠能减轻大鼠心肌缺血再灌注损伤;10 mmol/L羟丁酸钠则加重了脂质过氧化反应和心肌缺血再灌注损伤。
目的:比較不同劑量羥丁痠鈉對離體大鼠缺血再灌註損傷心肌脂質過氧化作用的影響。方法將24隻成年Wistar大鼠隨機分為4組(n=6):心肌缺血再灌註組(I/R組),1 mmol/L羥丁痠鈉組(RL組),2.5 mmol/L羥丁痠鈉組( RM組),10 mmol/L羥丁痠鈉組( RH組)。採用 Langendorff離體心髒缺血再灌註模型,四組均以K-H液平衡灌註10 min,再以K-H液及1、2.5、10 mmol/L羥丁痠鈉的K-H液分彆灌註10 min,然後全心停止灌註25 min,再分彆繼續灌註30 min。測定冠脈流齣液總乳痠脫氫酶( LDH)活性;灌註末,用2.5%戊二醛固定左室心肌組織,觀察心肌超微結構;留取心尖部心肌組織以檢測8-異前列腺素、超氧化物歧化酶(SOD)活性。結果與IR組比較,RL組8-異前列腺素含量、SOD及LDH活性差異均無統計學意義(P>0.05),超微結構也未見損傷減輕;RM組8-異前列腺素含量、SOD活性差異均無統計學意義(P>0.05),LDH活性差異有統計學意義(P<0.05),超微結構可見損傷減輕;RH組8-異前列腺素含量、LDH活性升高(P<0.05),SOD活性差異均無統計學意義(P>0.05),超微結構可見損傷加重。結論羥丁痠鈉(1、2.5 mmol/L)不能降低心肌缺血再灌註損傷大鼠的8-異前列腺素含量,抑製脂質過氧化反應;但是2.5 mmol/L羥丁痠鈉能減輕大鼠心肌缺血再灌註損傷;10 mmol/L羥丁痠鈉則加重瞭脂質過氧化反應和心肌缺血再灌註損傷。
목적:비교불동제량간정산납대리체대서결혈재관주손상심기지질과양화작용적영향。방법장24지성년Wistar대서수궤분위4조(n=6):심기결혈재관주조(I/R조),1 mmol/L간정산납조(RL조),2.5 mmol/L간정산납조( RM조),10 mmol/L간정산납조( RH조)。채용 Langendorff리체심장결혈재관주모형,사조균이K-H액평형관주10 min,재이K-H액급1、2.5、10 mmol/L간정산납적K-H액분별관주10 min,연후전심정지관주25 min,재분별계속관주30 min。측정관맥류출액총유산탈경매( LDH)활성;관주말,용2.5%무이철고정좌실심기조직,관찰심기초미결구;류취심첨부심기조직이검측8-이전렬선소、초양화물기화매(SOD)활성。결과여IR조비교,RL조8-이전렬선소함량、SOD급LDH활성차이균무통계학의의(P>0.05),초미결구야미견손상감경;RM조8-이전렬선소함량、SOD활성차이균무통계학의의(P>0.05),LDH활성차이유통계학의의(P<0.05),초미결구가견손상감경;RH조8-이전렬선소함량、LDH활성승고(P<0.05),SOD활성차이균무통계학의의(P>0.05),초미결구가견손상가중。결론간정산납(1、2.5 mmol/L)불능강저심기결혈재관주손상대서적8-이전렬선소함량,억제지질과양화반응;단시2.5 mmol/L간정산납능감경대서심기결혈재관주손상;10 mmol/L간정산납칙가중료지질과양화반응화심기결혈재관주손상。
Objective To compare the effects of three different doses of gamma-hydroxybutyrate on lipid per-oxidation in isolated rat hearts after myocardial ischemia-reperfusion. Methods Twenty-four adult Wistar rats were randomly divided into 4 groups ( 6 rats in each group ):ischemia-reperfusion group ( I/R group ) , I/R + gamma-hydroxybutyrate (1,2. 5,10 mmol/L) groups (RL,RM,RH groups). The isolated rat hearts were perfused with Lan-gendorff perfusion system. All the rat hearts were initially perfused with Krebs-Henseleit ( K-H) solution for 10 min, then respectively perfused with K-H solution dissolved no gamma-hydroxybutyrate,gamma-hydroxybutyrate (1,2. 5, 10 mmol/L) for 10 min followed by 25 min global ischemia and 30 min reperfusion. The total lactate dehydrogenase ( LDH) of the reperfusion solution,levels of 8-isoprostane and SOD activity of apex of hearts were determined. The left ventricular tissues were used for observing myocardial ultrastructure. Results The levels of 8-isoprostane, LDH and SOD activity in group RL did not significantly differ from I/R group ( P>0. 05 ) . The myocardial ultrastructure also showed that group RL cannot lessened the myocardial I/R injury. Although levels of 8-isoprostane and SOD activity in group RM did not significantly differ from those in I/R group (P>0. 05),the LDH activity differed significantly(P<0. 05). The microscopic examination indicated that group RM can alleviate the myocardial I/R injury,but compared with I/R group,levels of 8-isoprostane and LDH were raised significantly ( P <0. 05 ) , the myocardial ultrastructure was injuried more seriously. Conclusion Gamma-hydroxybutyrate (1,2. 5 mmol/L) cannot decrease the levels of 8-isoprostane or inhibit lipid peroxidation. But 2. 5 mmol/L Gamma-hydroxybutyrate can alleviate the myocardial I/R in-jury. While 10 mmol/L Gamma-hydroxybutyrate can exacerbated lipid peroxidation and myocardial ischemia-reperfu-sion injury.